Genetic recombination is an essential feature of normal meiosis and during repair of various types of DNA damage. As part of a program to understand the mechanisms of recombination and its genetic control, the timing and the location of recombination events are being evaluated by applying mathematical simulation procedures to biochemical data. DNA lesions can be used as markers in exchange processes where the lesions can be identified using enzymes which will nick the DNA, and thus reduce the size of the DNA. If recombination occurs, lesions induced in parental strands of DNA can become associated with newly synthesized DNA; therefore, as a result of recombination events, newly synthesized DNA can become sensitive to nicking enzymes. Using this approach, we have been able to predict the detectibility of exchanges by mathematical modeling, knowing the average number of lesions per parental molecule, and to relate exchanges to models for recombination. Biological results from E. coli, yeast, and mammalian cells are being evaluated using the mathematical simulation. In rad52 strains of yeast which are lacking in DNA repair, meiosis is defective. Cells accumulate rare single-strand interruptions in their chromosomal DNA during meiosis which are likely to be associated with recombination in wild type strains. To identify their frequencies in individual chromosomes and their distributions, we have utilized small probes to specific chromosomes. The chromosomal DNA is separated according to size on sucrose gradients and individual fractions are hybridized with the probe. We have utilized mathematical modeling to analyze the best positioning for a probe relative to the end of the chromosome in order to detect rare interruptions. The actual probing data were analyzed mathematically in terms of various models. The distribution of SSIs is clearly nonrandom which would indicate specificity of recombination sites in yeast.